Chronic heart failure is characterized by activation of neurohormonal systems in response to impaired cardiac function. These hormones maintain blood flow to vital organs acutely, but enventually cause disease progression. The past decade has seen a marked improvement in the effectiveness of therapy for this progressive disorder - primarily in the form of agents that improve autonomic imbalance and neurohormonal activation. One such approach is the use of angiotensin converting enzyme inhibition, which restores autonomic function and neurohormonal activity towards normal, improving quality of life and reducing the risk of death. Another approach is the use of adrenergic antagonists, one of which, carvedilol, is approved by the FDA for the treatment of chronic heart failure based on its ability to reduce the progression of the disease. However, the use of carvedilol will be limited because it is difficult to use and patients frequently suffer clinical deterioration early in the treatment before realizing long-term benefit. The need for agents to antagonize the activation of the sympathetic nervous system in chronic heart failure is irrefutable. The barriers to the use of beta-blockers emphasize the need to develop alternatives. Therefore, we propose to test whether a centrally acting sympatholytic drug, moxonidine, would improve clinical outcomes in patients with chronic heart failure. Patients will be randomly assigned to receive study medication, either SR moxonidine or placebo, titrated to a maximal dose of 1.5 mg PO BID. SR moxonidine is an I1-imidazoline receptor agonist, acting in the rostroventrolateral medulla, producing sympatholytic effects, which would serve to restore autonomic balance towards normal and reduce neurohormonal acativation. Although structurally related to clonidine, moxonidine differs by having significantly less a-2 receptor agonist effects. This is a randomized, double-blind, placebo-controlled, multicenter study in patients with chronic heart failure (symptomatic, NYHA Class II-IV). The primary objective is to compare the effect on survival of moxonidine to placebo therapy. Secondary objectives include the time to first occurrence of the combined endpoint of all-cause mortality and hospitalization due to worsening heart failure